SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway

Y. Zhang, L.-M. Zheng, C.-X. Wang, J.-M. Gu, S. Xue

Departments of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. renjixuesong@163.com

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• Cardiology

OBJECTIVE: To investigate whether SENP3 protects H9C2 cells from apoptosis triggered by H/R through the signal transducer and activator of transcription 3 (STAT3) pathway.

MATERIALS AND METHODS: Male C57BL mice were cultured and mouse models of myocardial I/RI were established. At the same time, cardiomyoblast H9C2 cell line of rat embryo was cultured. Reactive oxygen species (ROS) level was detected during H/R using 2’,7’-dichlorofluorescein diacetate (DCFH) kit. Apoptotic cells were checked by flow cytometry. The expressions of p-JAK2, JAK2, STAT3, p-STAT3, cleaved-caspase3 (c-caspase3), and Bcl/Bax were detected using Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR).

RESULTS: We revealed that SENP3 rose in mice of I/R group and in H9C2 cells following H/R with an increase in p-STAT3. Furthermore, increased expression of SENP3 was found to be dependent on the generation of ROS, as the SENP3 accumulation was inhibited by antioxidant (NAC). Inhibition of SENP3 suppressed the p-STAT3 expression, but promoted cell apoptosis, c-caspase3 expression, and Bcl/Bax ratio. Besides, SENP3 overexpression alleviated the cell apoptosis, which was abrogated by AG490.

CONCLUSIONS: SENP3 could protect H9C2 against H/R through enhancing JAK2/STAT3 pathway.

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